Our present results indicate that the content of lysoglycerophosphatides increases about 3.5 fold in the hearts of ground squirrels during hibernation. We have further demonstrated, by electron spin resonance spectroscopy, that the addition of lysolecithin (at the same molar percent found in hibernating hearts) to the phospholipids from active ground squirrels, increases the degree of disorder, or "fluidity" of the phospholipids, so a phase transition to a solid state does not occur at reduced temperatures. This evidence strongly suggests that an alternative mechanism of low temperature tolerance (approximately 1 C) may be to increase the content of lysoglycerophosphatides in cellular membranes, as opposed to increasing the degree of fatty acid unsaturation, as is characteristically observed in bacteria, plants and animals adapted for growth at low temperatures. Our primary objective is to examine this hypothetical mechanism in greater detail by (1), analyzing mitochondrial succinate oxidation as a function of temperature before and after the induction of lysoglycerophosphatides, (2), analyzing the temperature-activity characteristics of whole, perfused heart before and after lysoglycerophosphatide induction, and, (3) correlating the content of lyso-compounds determined by phospholipid analysis with the physiological function at reduced temperatures and the ultrastructural appearance as determined by electron microscopy. Furthermore, in order to relate precisely the degree of membrane-lipid fatty acid unsaturation and lysoglycerophosphatide content, with the capacity of the heart membranes of hibernating mammals to continue activity at reduced temperatures (approximately 1 C), our preliminary fatty acid analysis will be quantified by determining molar relationships of the fatty acids of the membrane phospholipids.